September 20, 2013

In Research

Copper identified as culprit in Alzheimer’s disease

Copper appears to be one of the main environmental factors that trigger the onset and enhance the progression of Alzheimer’s disease by preventing the clearance and accelerating the accumulation of toxic proteins in the brain. That is the conclusion of a Medical Center study appearing in the journal Proceedings of the National Academy of Sciences.

“It is clear that, over time, copper’s cumulative effect is to impair the systems by which amyloid beta is removed from the brain,” says Rashid Deane, a research professor in the Department of Neurosurgery, member of the Center for Translational Neuromedicine, and the lead author of the study. “This impairment is one of the key factors that cause the protein to accumulate in the brain and form the plaques that are the hallmark of Alzheimer’s disease.”

Copper’s presence in the food supply is ubiquitous. It’s found in drinking water carried by copper pipes, nutritional supplements, and in certain foods such as red meats, shellfish, nuts, and many fruits and vegetables. The mineral plays an important and beneficial role in nerve conduction, bone growth, the formation of connective tissue, and hormone secretion.

However, the new study shows that copper can also accumulate in the brain and cause the blood brain barrier— the system that controls what enters and exits the brain—to break down, resulting in the toxic accumulation of the protein amyloid beta, a byproduct of cellular activity. Using both mice and human brain cells Deane and his colleagues conducted a series of experiments that have pinpointed the molecular mechanisms by which copper accelerates the pathology of Alzheimer’s disease.

Device aims to help toilet train children with autism

A new device developed at the University is showing promise of reducing the time and effort required to toilet train children with autism and other developmental disabilities.

“We have research that shows it can take a family a year-anda- half to toilet train a child with autism or other developmental disability” says Daniel Mruzek, associate professor of pediatrics. “In the initial pilot, our device drastically reduced that time to just a few weeks.”

Mruzek and Stephen McAleavey, associate professor of biomedical engineering, used fairly common items to construct their toilet training device: sterile pads, a sensor, a Bluetooth-enabled transmitter, and an iPod. They received some help from Dan Hansen, a freshman computer science major, who wrote the software for the project.

When a drop of urine is detected on a pad, a signal is sent to the iPod, triggering a sound or piece of music. At the same time, an alarm is activated on an iPod being worn by a teacher or caregiver, who can then assist the child in using the toilet. If the child successfully uses the facilities, the iPod offers up a reward in the form of a game, song, or photo.

The device is an upgrade from a model they developed six years earlier. The University is collaborating with Vanderbilt University and Nationwide Children’s Hospital on a new round of clinical testing, which has just gotten under way.

Researchers optically levitate a glowing, nanoscale diamond

Optics researchers at the University have measured for the first time light emitted by photoluminescence from a nanodiamond levitating in free space. In a paper published in Optics Letters, researchers describe how they used a laser to trap nanodiamonds in space, and—using another laser— caused the diamonds to emit light at given frequencies.

The experiment, led by Nick Vamivakas, assistant professor of optics, demonstrates that it is possible to levitate diamonds as small as 100 nanometers (approximately a thousandth the diameter of a human hair) in free space, by using a technique known as laser trapping.

“Now that we have shown we can levitate nanodiamonds and measure photoluminescence from defects inside the diamonds, we can start considering systems that could have applications in the field of quantum information and computing,” Vamivakas says. He said an example of such a system would be optomechanical resonators— structures in which the vibrations of the system, in this case the trapped nanodiamond, can be controlled by light. “We are yet to explore this, but in theory we could encode information in the vibrations of the diamonds and extract it using the light they emit.”

Tracking Twitter may enhance monitoring of food safety

University researchers have developed a system that could tell you how likely it is for you to become ill if you visit a particular restaurant by “listening” to the tweets from other restaurant patrons.

Researchers say the system, nEmesis, can help people make more informed decisions, and it also has the potential to complement traditional public health methods for monitoring food safety, such as restaurant inspections. For example, it could enable what they call “adaptive inspections,” inspections guided in part by the real-time information that nEmesis provides.

The system combines machine-learning and crowdsourcing techniques to analyze millions of tweets to find people reporting food poisoning symptoms following a restaurant visit.

“The Twitter reports are not an exact indicator—any individual case could well be due to factors unrelated to the restaurant meal—but in aggregate the numbers are revealing,” says Henry Kautz, chair of the Department of Computer Science and coauthor of the paper. In other words, a “seemingly random collection of online rants becomes an actionable alert,” which can help detect cases of food borne illness in a timely manner, according to Kautz.

Study: No link between mercury exposure and autism-like behaviors

A study from Medical Center researchers that draws upon more than 30 years of research in the Republic of Seychelles reports that there is no association between prenatal mercury exposure and autism-like behaviors.

“This study shows no evidence of a correlation between low level mercury exposure and autism spectrum–like behaviors among children whose mothers ate, on average, up to 12 meals of fish each week during pregnancy,” says Edwin van Wijngaarden, associate professor in the Department of Public Health Sciences and lead author of the study which appears online in the journal Epidemiology. “These findings contribute to the growing body of literature that suggest that exposure to the chemical does not play an important role in the onset of these behaviors.”

The debate over fish consumption has long created a dilemma for expecting mothers and physicians. Fish are high in beneficial nutrients such as selenium, vitamin E, lean protein, and omega-3 fatty acids; the latter are essential to brain development. At the same time, exposure to high levels of mercury has been shown to lead to developmental problems, leading to the claim that mothers are exposing their unborn children to serious neurological impairment by eating fish during pregnancy. Despite the fact that the developmental consequences of low level exposure remain unknown, some organizations, including the U.S. Food and Drug Administration, have recommended that pregnant women limit their consumption of fish.

Biologists identify chemical behind rodent’s cancer resistance

University researchers have discovered the chemical that seems to make naked mole rats cancer-proof.

The findings, published in Nature, could help lead to new cancer treatments in people, say study authors Andrei Seluanov, assistant professor of biology, and Vera Gorbunova, professor of biology.

Naked mole rats are small, hairless, subterranean rodents that have never been known to get cancer, despite having a 30-year lifespan. The research group led by Seluanov and Gorbunova discovered that a key element of the resistance to cancer is that their tissues are very rich with high molecular weight hyaluronan (HMW-HA), a compound known to make tissue supple and to aid in the healing process. The Rochester team also identified a gene, named Has2, responsible for making HMW-HA in the naked mole rat. Surprisingly, the naked mole rat gene was different from the same gene in all other animals.

Scientists coax brain to regenerate cells

Researchers have been able to mobilize the brain’s native stem cells to replenish a type of neuron lost in Huntington’s disease.

In the study, which appears in the journal Cell Stem Cell, Rochester scientists were able to both trigger the production of new neurons in mice with the disease and show that the new cells successfully integrated into the brain’s existing neural networks, dramatically extending the survival of the treated mice.

“This study demonstrates the feasibility of a completely new concept to treat Huntington’s disease, by recruiting the brain’s endogenous neural stem cells to regenerate cells lost to the disease,” says neurologist Steve Goldman, codirector of Rochester’s Center for Translational Neuromedicine. Huntington’s disease is an inherited neurodegenerative disease characterized by the loss of a specific cell type called the medium spiny neuron, a cell that is critical to motor control. The disease, which affects some 30,000 people in the U.S., results in involuntary movements, problems with coordination, and, ultimately, in cognitive decline and depression. There is currently no way to slow or modify the fatal disease.